Molecular mechanisms linking adipose tissue browning to reduced cardiovascular risk

Le résumé fourni par la source

Recent research elucidates the complex molecular mechanisms linking adipose tissue (AT) browning to improved metabolic and cardiovascular health. Pro-inflammatory signaling pathways, such as NLRP3 inflammasome, TLR4, and NF-κB, typically inhibit browning, whereas their disruption promotes it. Conversely, anti-inflammatory pathways mediated by IL-4, IL-13, and M2 macrophages stimulate browning and are associated with enhanced glucose tolerance and insulin sensitivity. Mitochondrial regulation is central to this process, with UCP-1 and PGC1-α as key effectors. Interventions like ASK-1 knockout, nitrate, and melatonin have increased thermogenesis and improved metabolic outcomes in preclinical models. A limited number of studies directly measuring cardiovascular endpoints report improved endothelial function, reduced hypertension, reduced atherosclerotic plaque inflammation with attenuated atherosclerosis progression and decreased liver steatosis, suggesting significant cardioprotective potential. However, most evidence remains preclinical, derived from in vitro and animal studies. Interpretations are complicated by context-dependent effects, such as variable responses in IL-6 signaling. The current literature indicates that white AT browning mitigates inflammation and improves cardiometabolic health through multiple pathways that include key atherosclerosis-related risk factors; direct clinical confirmation is needed. Future research should prioritize human validation of preclinical findings to determine sex-specific responses, identify target patient populations, particularly those at high risk of atherosclerotic cardiovascular disease, and develop AT-targeted therapies with fewer off-target cardiovascular and systemic adverse effects.

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